Published in:
01-11-2006 | Short Communication
Sympathetic nerve hyperactivity in non-diabetic offspring of patients with type 2 diabetes mellitus
Published in: Diabetologia | Issue 11/2006
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Aims/hypothesis
Type 2 diabetes mellitus with hyperinsulinaemia is a state of sympathetic nerve hyperactivity, which can develop subsequently in non-diabetic first-degree offspring of patients with type 2 diabetes. Although both type 2 diabetes and sympathetic activation are major cardiovascular risk factors, the level of sympathetic nerve activity is as yet unknown in offspring of type 2 diabetic patients who are ostensibly normal. We therefore sought to quantify sympathetic nerve activity and its relationship to plasma insulin levels in ostensibly normal offspring of patients with type 2 diabetes, relative to a matched normal control group with no family history of type 2 diabetes.
Subjects and methods
In two closely matched groups comprising 23 non-diabetic offspring of type 2 diabetic patients and 23 normal control individuals we measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multi-unit bursts of MSNA and single units of MSNA (s-MSNA) with defined vasoconstrictor properties.
Results
In offspring of type 2 diabetic patients, the fasting plasma levels of insulin (7.4±0.80 μU/ml) and s-MSNA (45±3.2 impulses/100 beats) were greater (p<0.009 and p<0.003) than those in control persons (4.6±0.76 μU/ml and 32±3.1 impulses/100 beats, respectively). MSNA bursts and derived insulin resistance followed similar trends. Sympathetic nerve activity was significantly correlated to insulin levels (p<0.0002) and resistance (p<0.0001) in offspring of type 2 diabetic patients, but not in control subjects.
Conclusions/interpretation
Sympathetic activation occurred in normal non-diabetic offspring of patients with type 2 diabetes in proportion to their plasma insulin levels. Our data indicate the presence of a mechanistic link between hyperinsulinaemia and sympathetic activation, both of which could play a role in the subsequent development of cardiovascular risk factors.